Closely Related Influenza Viruses Induce Contrasting Respiratory Tract Immunopathology
Identifieur interne : 000D73 ( Pmc/Curation ); précédent : 000D72; suivant : 000D74Closely Related Influenza Viruses Induce Contrasting Respiratory Tract Immunopathology
Auteurs : Vy L. Le [États-Unis] ; Cynthia L. Courtney [États-Unis] ; John Steel [États-Unis] ; Richard W. Compans [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2013.
Abstract
The swine-origin H1N1 virus which emerged in 2009 resulted in the first influenza pandemic of the 21st century. Although the majority of infections were moderate, a significant proportion of infections were severe and characterized by acute respiratory distress syndrome and pulmonary edema. We compared two isolates from the 2009 H1N1 pandemic; A/California/07/09 (CA/07) and A/Netherlands/602/09 (NL/602) viruses that share greater than 99% sequence identity. Though genetically similar, these viruses exhibit contrasting pathological effects. Mice that were infected with 800 plaque forming unit (PFU) of CA/07 virus rapidly lost weight, which was concurrent with detection of high pulmonary concentrations of MCP-1, MIG, IP-10 and TIMP-1. Initially, severe bronchiolar epithelial necrosis and acute respiratory distress was observed, followed by marked bronchiolar epithelial hyperplasia. Mononuclear cell infiltration was initially localized to perivascular and peribronchiolar interstitium and then spread to adjacent alveoli. Infiltrating cells were phenotypically CD11bhi, F4/80lo. In contrast, when mice were infected with 800 PFU of NL/602 virus, minimal weight loss was observed, and concentrations of cytokines in the lung were significantly lower. Inflammation was primarily restricted to the bronchioles and perivascular interstitium with minimal spread to alveoli. Infiltrating cells include foamy macrophages and surface markers were characterized as CD11blo/-, F4/80hi. These two genetically similar viruses can be useful strains with which to investigate immune-regulatory determinants of pathogenesis of influenza virus.
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DOI: 10.1371/journal.pone.0076708
PubMed: 24086762
PubMed Central: 3784437
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Closely Related Influenza Viruses Induce Contrasting Respiratory Tract Immunopathology</title><author><name sortKey="Le, Vy L" sort="Le, Vy L" uniqKey="Le V" first="Vy L." last="Le">Vy L. Le</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia</wicri:regionArea></affiliation></author><author><name sortKey="Courtney, Cynthia L" sort="Courtney, Cynthia L" uniqKey="Courtney C" first="Cynthia L." last="Courtney">Cynthia L. Courtney</name><affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>Department of Pathology and Laboratory Medicine, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, Emory University, School of Medicine, Atlanta, Georgia</wicri:regionArea></affiliation></author><author><name sortKey="Steel, John" sort="Steel, John" uniqKey="Steel J" first="John" last="Steel">John Steel</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia</wicri:regionArea></affiliation></author><author><name sortKey="Compans, Richard W" sort="Compans, Richard W" uniqKey="Compans R" first="Richard W." last="Compans">Richard W. Compans</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24086762</idno><idno type="pmc">3784437</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784437</idno><idno type="RBID">PMC:3784437</idno><idno type="doi">10.1371/journal.pone.0076708</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000D73</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000D73</idno><idno type="wicri:Area/Pmc/Curation">000D73</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000D73</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Closely Related Influenza Viruses Induce Contrasting Respiratory Tract Immunopathology</title><author><name sortKey="Le, Vy L" sort="Le, Vy L" uniqKey="Le V" first="Vy L." last="Le">Vy L. Le</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia</wicri:regionArea></affiliation></author><author><name sortKey="Courtney, Cynthia L" sort="Courtney, Cynthia L" uniqKey="Courtney C" first="Cynthia L." last="Courtney">Cynthia L. Courtney</name><affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>Department of Pathology and Laboratory Medicine, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Laboratory Medicine, Emory University, School of Medicine, Atlanta, Georgia</wicri:regionArea></affiliation></author><author><name sortKey="Steel, John" sort="Steel, John" uniqKey="Steel J" first="John" last="Steel">John Steel</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia</wicri:regionArea></affiliation></author><author><name sortKey="Compans, Richard W" sort="Compans, Richard W" uniqKey="Compans R" first="Richard W." last="Compans">Richard W. Compans</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia</wicri:regionArea></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The swine-origin H1N1 virus which emerged in 2009 resulted in the first influenza pandemic of the 21<sup>st</sup> century. Although the majority of infections were moderate, a significant proportion of infections were severe and characterized by acute respiratory distress syndrome and pulmonary edema. We compared two isolates from the 2009 H1N1 pandemic; A/California/07/09 (CA/07) and A/Netherlands/602/09 (NL/602) viruses that share greater than 99% sequence identity. Though genetically similar, these viruses exhibit contrasting pathological effects. Mice that were infected with 800 plaque forming unit (PFU) of CA/07 virus rapidly lost weight, which was concurrent with detection of high pulmonary concentrations of MCP-1, MIG, IP-10 and TIMP-1. Initially, severe bronchiolar epithelial necrosis and acute respiratory distress was observed, followed by marked bronchiolar epithelial hyperplasia. Mononuclear cell infiltration was initially localized to perivascular and peribronchiolar interstitium and then spread to adjacent alveoli. Infiltrating cells were phenotypically CD11b<sup>hi</sup>, F4/80<sup>lo</sup>. In contrast, when mice were infected with 800 PFU of NL/602 virus, minimal weight loss was observed, and concentrations of cytokines in the lung were significantly lower. Inflammation was primarily restricted to the bronchioles and perivascular interstitium with minimal spread to alveoli. Infiltrating cells include foamy macrophages and surface markers were characterized as CD11b<sup>lo/-</sup>, F4/80<sup>hi</sup>. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">PLoS One</journal-id><journal-id journal-id-type="iso-abbrev">PLoS ONE</journal-id><journal-id journal-id-type="publisher-id">plos</journal-id><journal-id journal-id-type="pmc">plosone</journal-id><journal-title-group><journal-title>PLoS ONE</journal-title></journal-title-group><issn pub-type="epub">1932-6203</issn><publisher><publisher-name>Public Library of Science</publisher-name><publisher-loc>San Francisco, USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24086762</article-id><article-id pub-id-type="pmc">3784437</article-id><article-id pub-id-type="publisher-id">PONE-D-13-23636</article-id><article-id pub-id-type="doi">10.1371/journal.pone.0076708</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Closely Related Influenza Viruses Induce Contrasting Respiratory Tract Immunopathology</article-title><alt-title alt-title-type="running-head">Influenza A Virus Induced Pathogenesis</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Le</surname><given-names>Vy L.</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><contrib contrib-type="author"><name><surname>Courtney</surname><given-names>Cynthia L.</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Steel</surname><given-names>John</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Compans</surname><given-names>Richard W.</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib></contrib-group><aff id="aff1"><label>1</label><addr-line>Department of Microbiology and Immunology, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></aff><aff id="aff2"><label>2</label><addr-line>Department of Pathology and Laboratory Medicine, Emory University, School of Medicine, Atlanta, Georgia, United States of America</addr-line></aff><contrib-group><contrib contrib-type="editor"><name><surname>Boon</surname><given-names>Adrianus CM</given-names></name><role>Editor</role><xref ref-type="aff" rid="edit1"></xref></contrib></contrib-group><aff id="edit1"><addr-line>Washington University School of Medicine, United States of America</addr-line></aff><author-notes><corresp id="cor1">* E-mail: <email>vlle@emory.edu</email> (VLL); <email>rcompan@emory.edu</email> (RWC)</corresp><fn fn-type="COI-statement"><p><bold>Competing Interests: </bold>The authors have declared that no competing interests exist.</p></fn><fn fn-type="con"><p>Conceived and designed the experiments: VLL. Performed the experiments: VLL CLC. Analyzed the data: VLL CLC. Contributed reagents/materials/analysis tools: JS. Wrote the manuscript: VLL. Review of manuscript: JS RWC. </p></fn></author-notes><pub-date pub-type="collection"><year>2013</year></pub-date><pub-date pub-type="epub"><day>26</day><month>9</month><year>2013</year></pub-date><volume>8</volume><issue>9</issue><elocation-id>e76708</elocation-id><history><date date-type="received"><day>6</day><month>6</month><year>2013</year></date><date date-type="accepted"><day>24</day><month>8</month><year>2013</year></date></history><permissions><copyright-statement>© 2013 Le et al</copyright-statement><copyright-year>2013</copyright-year><copyright-holder>Le et al</copyright-holder><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.</license-p></license></permissions><abstract><p>The swine-origin H1N1 virus which emerged in 2009 resulted in the first influenza pandemic of the 21<sup>st</sup> century. Although the majority of infections were moderate, a significant proportion of infections were severe and characterized by acute respiratory distress syndrome and pulmonary edema. We compared two isolates from the 2009 H1N1 pandemic; A/California/07/09 (CA/07) and A/Netherlands/602/09 (NL/602) viruses that share greater than 99% sequence identity. Though genetically similar, these viruses exhibit contrasting pathological effects. Mice that were infected with 800 plaque forming unit (PFU) of CA/07 virus rapidly lost weight, which was concurrent with detection of high pulmonary concentrations of MCP-1, MIG, IP-10 and TIMP-1. Initially, severe bronchiolar epithelial necrosis and acute respiratory distress was observed, followed by marked bronchiolar epithelial hyperplasia. Mononuclear cell infiltration was initially localized to perivascular and peribronchiolar interstitium and then spread to adjacent alveoli. Infiltrating cells were phenotypically CD11b<sup>hi</sup>, F4/80<sup>lo</sup>. In contrast, when mice were infected with 800 PFU of NL/602 virus, minimal weight loss was observed, and concentrations of cytokines in the lung were significantly lower. Inflammation was primarily restricted to the bronchioles and perivascular interstitium with minimal spread to alveoli. Infiltrating cells include foamy macrophages and surface markers were characterized as CD11b<sup>lo/-</sup>, F4/80<sup>hi</sup>. These two genetically similar viruses can be useful strains with which to investigate immune-regulatory determinants of pathogenesis of influenza virus.</p></abstract><funding-group><funding-statement>This study was supported by National Institutes of Health (NIH) grants A1074579, P51OD11132 and a Queensland Institute of Medical Research-Australian Center for Vaccine Development and Emory Vaccine Center (ACVD-EVC) Pilot projects. V.L. Le is supported by NIH grant T32-A1074492 and J. Steel is supported through a pilot project from the Centers for Excellence in Influenza Research and Surveillance (CEIRS) contract number HHSN266200700006C. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.</funding-statement></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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